IL-10 Is a Negative Regulatory Factor of CAWS-Vasculitis in CBA/J Mice as Assessed by Comparison with Bruton’s Tyrosine Kinase-Deficient CBA/N Mice
Author(s) -
Noriko N. Miura,
Motohiko Komai,
Yoshiyuki Adachi,
Naoki Osada,
Yosuke Kameoka,
Kazuo Suzuki,
Naohito Ohno
Publication year - 2009
Publication title -
the journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.737
H-Index - 372
eISSN - 1550-6606
pISSN - 0022-1767
DOI - 10.4049/jimmunol.0802484
Subject(s) - vasculitis , candida albicans , immunology , bruton's tyrosine kinase , biology , systemic vasculitis , medicine , tyrosine kinase , microbiology and biotechnology , pathology , biochemistry , receptor , disease
Candida albicans water-soluble fraction (CAWS), a mannoprotein-beta-glucan complex obtained from the culture supernatant of C. albicans NBRC1385, exhibits vasculitis-inducing activity (CAWS-vasculitis) in mice. The sensitivity to CAWS-vasculitis varies greatly among mouse strains. This study examined the factors contributing to or inhibiting CAWS-vasculitis using CAWS-vasculitis-resistant CBA/J mice and Bruton's tyrosine kinase-deficient CBA/N mice, which is a CAWS-vasculitis-sensitive strain that has the same origin as CBA/J mice. After stimulation with various kinds of pathogen-associated molecular patterns, the production of inflammatory cytokines IL-6 and IFN-gamma was induced in CBA/N mice, whereas that of immunosuppressive IL-10 was induced in CAWS-vasculitis-resistant CBA/J mice. Furthermore, the production of tissue inhibitor of metalloproteinase 1, an endogenous matrix metalloproteinase inhibitor, was observed in CBA/J mice. The results strongly suggest that the difference in the production of these cytokines is closely linked to the development of CAWS-vasculitis.
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